Diagnosis of thrombophilia and control of antithrombotic therapy

The doctrine of thrombophilia allows you to select a number of factors and criteria thrombogenic risk, control of which is important in the examination and treatment of the patient population.

Rheological and cytological indicators

The risk of thrombosis increases sharply with increasing viscosity of the blood and plasma, in this connection, risk factors include:

  • policitemiю (increase in the number of red blood cells due to myeloproliferative process);
  • symptomatic erythrocytosis (respiratory failure, kidney and other.);
  • increase in hematocrit;
  • slowing the ESR;
  • increase in plasma viscosity at hyperfibrinogenemia;
  • paraproteinaemias (multiple myeloma, Waldenstrom's disease);
  • krioglobulinemin (immunocomplex disease);
  • elevation of plasma fibronectin.

The increase in volume and change in the shape of red blood cells as a factor of thrombogenicity have independent value. In these cases the deformabilnost erythrocytes during passage through capillaries, It is leading to stasis and promotes thrombogenicity. Established, that the increase in erythrocyte 10 % It leads to an increase in resistance to blood flow in the capillaries on 100 %.

For this reason, an important factor is the thrombogenic violation of capillary physiological hemodilution, which in the healthy body hematocrit capillaries is reduced to 32-35 % (the remaining red blood cells "reset" through the shunt from arterioles to veins). Violation of capillary hemodilution occurs in shock and other types of acute hypovolemia, as well as a variety of other severe conditions.

Thrombophilia is developed for all types of hyperthrombocytosis, especially in combination with eritremii, whereby the necessary control of the content of thrombocytes in the blood.

The factors include the risk of thrombogenic increasing the spontaneous aggregation of platelets and their aggregation when exposed to low doses of ADP and epinephrine, as well as more intense spreading of these cells on the foreign surface.

A number of thrombophilia characterized increase the content of von Willebrand factor and decreased revenues from endothelial prostacyclin. These indicators, as well as a violation of the vascular activation of fibrinolysis, reflect inferiority and decreased vascular endothelial thromboresistance.

Reducing plasma antithrombin III and enhancement of its geparinorezistentnosti, vыyavlyaemoe thrombin or geparinovыm testom, less accurate, tolerance test to heparin - highly thrombogenic signs of danger or existing massive intravascular coagulation. Such a violation is observed in hereditary thrombophilia and secondarily with heavy consumption of antithrombin III, its accelerated metabolism (including a result of treatment with heparin, with associated thrombosis rebound) and etc.

In a number of thrombophilia and venous thromboembolism observed hypercoagulation (on the APTT, Permission, tromboelastogramma). Prothrombin index in this respect is particularly informative, because it detects the activation of factor VII, which closed various mechanisms run the coagulation cascade.

However, there are many of thrombophilia, not proceeding with increased, but with reduced blood clotting. These include the tendency to thrombosis deficiency of factor XII, prekallikreina (obviously, by virtue of the simultaneous weakening of the internal mechanism of activation of fibrinolysis), quite a number of thrombogenic disfibrinogenemy, accompanied by the extension as a common clotting time, and thrombin time and reptilazovogo, and etc. Therefore hypocoagulation is not in itself evidence of the absence of thrombogenic danger, and often indicates the presence of the latter.

Described multiple thrombosis in hereditary protein deficiency C and S.

Violations of fibrinolysis in many cases combined with high thrombogenic risk. The most informative in this regard slowing euglobulin lysis, weak activation of his trial at the cuff, weakening XIIa-kallikreinzavisimogo lysis, reduction of the plasminogen activator and the plasma and in the vascular wall.

With the above disorders are also associated rebound thromboembolism, arising from improper treatment of fibrinolytic drugs - streptokinase and urokinase.

Following intravenous administration of these drugs in high doses initially sharply activated fibrinolysis, whereby the majority of circulating plasminogen is converted to the active enzymeplasmin. The last is eliminated from the bloodstream, whereby during the next 12-24 hours, the level of plasminogen in the blood is very low (10-25% below the norm). With daily repeated administration of fibrinolytic gipoplazminemiya supported, which leads to increased thrombotic events. To prevent such a condition or entered a relatively small dose fibrinolysis activators (to 150000 IU streptokinase per day), a decline in plasminogen compensated jet transfusion of fresh frozen plasma or drugs plasminogen.

Recently created thrombolytic drugs (tissue-type activator, acylated streptokinase and urokinase), activating plasmin almost exclusively in thrombi, and not in circulation. When using these products the level of plasminogen in plasma hardly reduces thrombogenic and hazard. In the lysis of blood clots is very active.

Accounting for the above parameters to determine the shape and outline of thrombophilia tactics pathogenetic treatment of patients.

Control of antithrombotic therapy

Treatment with anticoagulants of indirect action

Treatment with anticoagulants of indirect action controlled by two tests - prothrombin (It gives an idea of ​​the suppression of the synthesis of three of the four K-factors vitaminozavisimyh) and activated partial thromboplastin time (controls the reduction of factor IX).

Valid, does not lead to hemorrhagic risk, It is to increase the performance in 2- 2,5 times. In the first days of treatment monitoring is carried out daily, then (After determining the optimal dose) - In one day, and when moving to the small maintenance doses - once in 7-10 days.

Antytrombotycheskyy effect antykoahulyantov indirect actions It manifested in their long reception even in doses, in which the prothrombin index and aPTT almost reduced. This is due to the favorable effect of anticoagulants on the synthesis of antithrombin III, prostacyclin, tkanevogo activator fibrinolysis.

Treatment with heparin

Treatment with heparin often controlled by activated partial thromboplastin time, Although using different samples kephaline sensitivity of the test may be uneven. Years of experience, that reliable monitoring can be carried out by a reduced or autokoagulyatsionnogo mikrokoagulyatsionnogo (the taking of blood from a finger) test. There are also study clotting time (Lee-White) and thromboelastography, performed at the bedside.

One of the most important conditions of treatment - uniform anticoagulant effect of the drug during the day, that is unattainable with intravenous administration of a single dose it every 3-4 hours. So show room drip intravenous heparin, and repeated subcutaneous administration in the abdomen by 5000 2-4 IU twice daily. For intravenous drip dose of heparin often fluctuates from 500 to 1000 U / h; if necessary, added subcutaneous injection.

Necessary to control the level of antithrombin III and timely correction of its plasma transfusions. Otherwise, the effect of the drug hypocoagulation, sufficient in the first day of treatment, maybe in a few days it is much weakened. In such a beam effective correction often achieved not increasing doses of heparin, and administration of drugs, containing antithrombin III (always jet, not a drip!).

Bleeding in the treatment of heparin It may also occur with a slight increase clotting time (optimal level - an increase by 2-2.5 times aPTT, except in cases of extracorporeal circulation and hemodialysis, when large doses). This is due to the occasional heparin in patients with thrombocytopenia. Therefore, it is also important to monitor the content of blood platelets.

Treatment thrombolytic

Treatment thrombolytic controlled thrombin time, determining the concentration of fibrinogen in plasma plasminogen and reserve. This may be used micromethods, t. it is. tests, performed with whole blood, taken from the finger. These methods are applied in the neonatologist. A small amount of plasma can be obtained by centrifuging the blood in the U-shaped folded plastic tubes with lumen diameters 1,5- 2 mm.

The most difficult is the selection of a dose of heparin in the treatment of disseminated intravascular coagulation, because the effect of the drug accumulates in the highly dynamic clotting, caused by a pathological process. In such cases generally should be guided by clinical situation - the degree of blockade of microcirculation and hazard (or gain) uncontrolled profuse bleeding, the degree of existing anticoagulation, etc.. d.

Study of the hemostatic system in the preoperative period

Evaluation of patients before surgery is performed to determine the risk of developing during and after it not only heavy bleeding complications, and thromboembolic events and DIC, who dominate the postoperative hemostasis disorders.

The tendency to hemorrhage It can be identified by the following set of common and public research:

  • определения времени кровотечения;
  • определения количества тромбоцитов в крови, их агрегации (визуально на стекле) под влиянием ристомицина, а также трех основных коагуляционных тестов — активированного парциального тромбопластинового, протромбинового и тромбинового.

Выявить опасность развития тромбозов и ДВС-синдрома позволяет исследование гепаринорезистентности плазмы (тромбин-гепариновый тест, тест толерантности плазмы к гепарину), содержания в ней РФМК (ethanol, протаминсульфатный и ортофенантролиновый тесты), определение эуглобулинового времени лизиса.

Профилактика тромботических осложнений путем подкожного введения гепарина (by 5000 ЕД через каждые 12 ч в течение всего послеоперационного периода) в сочетании с одновременным назначением эрготамина (at conventional doses) не требует специального лабораторного контроля.

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